Impact of Obesity on the Respiratory System - PowerPoint Presentation

Slide1

Impact of Obesity on the Respiratory System

Matthew J. Baugh, M.D.

Pulmonary and Critical Care Medicine

DuPage

Medical GroupSlide2

Topics

Effects of obesity on lung volumes and function

Asthma and

o

besity

Obstructive sleep apnea

Obesity Hypoventilation Syndrome

Obesity and venous thromboembolismSlide3

how does obesity affect the lungs?Slide4

Clevelandclinicmeded.com

Reductions of ERV and FRC

Reduced chest wall compliance

Reductions in TLC, VC, and RV can be seen in morbid obesitySlide5

Airway resistance increases as BMI increases

Overall increased work of breathing due to increased forces needed to inflate the lungs (can be 60-250% higher)

Weakening of respiratory muscles (impaired diaphragmatic function)Slide6

Oxygenation in obese patients

In many patients PaO2 is normal or mildly reduced

Hypoxemia can occur in severe obesity and OHS

Premature airway closure = V/Q mismatch

Hypoventilation further contributes in OHSSlide7

Control and pattern of breathing in obesity

Obese patients often adapt a “rapid and shallow” breathing pattern

Resting respiratory rate can be 40% higher in obese patients

Ventilatory

drive can be reduced in patients with OHS

Diminished response to rising CO2

Leptin

resistance?Slide8

Dyspnea

Very frequent symptom of patients with obesity, especially with exertion

Patients also have other comorbid diseases such as cardiac disease which can contribute

Obesity has been shown to increase risk for asthma and VTESlide9

Obesity and asthmaSlide10

Epidemiologic studies show 1.5 to 3.5x higher risk of asthma in obesity

Being overweight increases risk by 50-70%

Sin et al 2007Slide11

Beuther

, et al 2006Slide12

Obesity and Asthma

Leptin

resistance leading to airway

hyperresponsiveness

Increased likelihood of

atopy

in obese

Chronic inflammatory state

Adipokines

:

leptin

(high) and

adiponectin

(low) may be involved in pulmonary inflammation.

? Role of adipose macrophages and alveolar macrophagesSlide13

(Proceedings of American Thoracic Society, 2010)Slide14

Asthma Control

Obese patients with asthma have more severe symptoms and increased medication use (even after adjustment for age, sex, race, income, education)

Obesity increases bronchodilator use by 94%

Less response to inhaled steroids and inhaled steroid/long-acting bronchodilator combos

Increase risk of asthma-related hospitalizations

Weight loss leads to improvement in asthma symptoms and control.

Taylor, et al. Thorax 2008Slide15

Asthma treatment

Weight loss (obviously)

Exercise

Treatment of comorbid conditions which are also associated with asthma and obesity

GERD

OSA

Prednisone only when necessarySlide16

Obesity and obstructive sleep apneaSlide17

Prevalence of OSA

2-5%, although studies in USA up to 20-30%

>40% in Obese

(Punjabi et al)

(Lopez et al)

BMI

% OSA

25-34.9

33.33

35-39.9

71.43

40-49.9

73.48

50-59.9

76.67

60+

94.83Slide18

OSA pathophysiology

Increased tissue thickness of tongue, pharyngeal soft tissues leading obstruction of the passage to the trachea

Relaxation of protective muscles of the airway during sleepSlide19

Other risk factors

Age

Gender (Male>Female)

Craniofacial anatomy

Neck circumference (>17in for men, > 16 in for women)

Nasal congestion

Tobacco use

Family historySlide20

Cardiovascular effects of OSA

Independent risk factor for hypertension

Higher risk depending on severity

OSA is common in drug-resistant hypertension

Treatment with CPAP results in small reduction in BP (but not as much as BP meds)

BP may not improve with treatment in those with long-standing hypertensionSlide21

Cardiovascular effects of OSA

Myocardial infarction

Severe OSA associated with an increase risk of fatal and nonfatal myocardial infarction

Treatment with CPAP lowers risk of MI

Incidence of MI no different in treated OSA vs. no OSA

(Marin et al)Slide22

Cardiovascular effects of OSA

Atrial fibrillation

Studies involving 24 hour

H

olter

monitoring have shown 3x higher risk of AF in patients with OSA compared to general population

25% higher risk for recurrent AF after

cardioversion

or ablation

Treatment with CPAP reduces risk of recurrence after

cardioversion

/ablation

(

Guilleminault

et al)

(Ng et al)Slide23

Cardiovascular effects of OSA

Congestive heart failure

-men with AHI > 30 were 58% more likely to develop HF than men without OSA

Sudden cardiac death

More common in patients with moderate to severe OSASlide24

Cardiovascular effects of OSA

Pulmonary hypertension

20-33% of patients with moderate to severe OSA have pulmonary hypertension

Degree of PH is usually mild unless other coexisting lung diseases present.

Treatment with CPAP lowers mean PA pressures.

(

Sanner

et al)Slide25

(Bradley, et al.)Slide26

OSA and the Central Nervous System

Stroke

OSA is independently associated with increased risk of stroke (as well as through its association with other risks such as AF and HTN)

Stroke survivors with moderately severe OSA have increased risk of early death

Treatment with CPAP improves acute stroke outcomes at 30 days compared to no treatment

Seizures and seizure controlSlide27

2x increased risk of motor vehicle accidents in those with OSASlide28

OSA and the Endocrine system

OSA is an independent risk factor for the development of DM

This risk is present even after adjusting for body mass index.

Patients with severe OSA (AHI>30) have 30% higher risk of developing diabetes than in patients without OSASlide29

OSA and Nonalcoholic Fatty Liver Disease (NAFLD)

OSA associated with 2-3x increased risk for NAFLD, independent of BMI

NAFLD can progress to cirrhosis over timeSlide30

Perioperative complications with OSA

Difficult intubation

Postoperative respiratory depression from anesthetics and analgesics

Higher risk of postoperative

reintubation

Higher risk of cardiac arrhythmias

Increased hospital length of stay, ICU length of staySlide31

Screening for OSA

Screening questionnaires

STOP-BANG

Mild OSA (AHI>5):

Sens

84%, Spec 56%

Mod-Severe OSA (AHI>15):

Sens

93% Spec 43%

Sleep Apnea Clinical Score (SACS)

Berlin QuestionnaireSlide32

S

noring

(loud enough to be heard through closed doors; bed partner elbows you at night)

T

ired

(feeling Tired, Fatigue, or Sleepiness during the daytime, falling asleep while driving)

O

bserved

(observed episodes of stopping breathing, gasping or choking during sleep)

P

ressure

(being treated for high blood pressure)

B

MI

(BMI >35)

A

ge

(Age > 50)

N

eck size large

(Shirt collar >17 inches males, > 16 inches females)

G

ender=Male

Low Risk = 0-2 Intermediate Risk = 3-4 High Risk = 5-8 Slide33

Diagnosis of OSA

Other symptoms

Restless sleep / frequent awakenings

Morning headaches

Poor concentration

Nocturia

(occurs in 50% of patients with OSA)

OSA leads to increased secretion of atrial natriuretic peptideSlide34

EPWORTH SCORE> 10 = EXCESSIVE SLEEPINESSSlide35

Polysomnography

First line diagnostic study for OSA

Measured variables

EEG and EMG for monitoring of sleep stages

Respiratory effort

Airflow

O2 saturation

EKG

Limb movement and body positionSlide36

OSA Severity

Apnea hypopnea index (average number of apneas and hypopneas per hour of sleep)

Mild OSA

AHI 5-15

Moderate OSA

AHI >15-30

Severe OSA

AHI>30Slide37

Treatment

Weight loss and exercise

CPAP (continuous positive airway pressure)

Significantly improves sleepiness

Improvements in quality of life

Improvements in cognitive function

Improves systemic blood pressure

Indications for CPAP

AHI>15 (moderate OSA)

AHI 5-15 with excessive sleepiness, impaired cognitive function, mood disorders, insomnia,

cardiovascular disease or stroke Slide38

CPAP

(continuous positive airway pressure)

Utilizes pressure to provide a pneumatic splint to maintain airway patency

More than 100 different mask options to customize treatment to an individual patientSlide39

Effects of weight loss on OSA

Reduction of weight (BMI) can lead to a reduction in AHI, associated with improvements in sleepiness & QOL (Norman, et al 2000)

Weight loss in morbidly obese patients has been shown to convert non-positional OSA to positional OSA; obviating need for CPAPSlide40

Bariatric surgery and OSA

Many patients will have improvement or even resolution of OSA after bariatric surgery

AHI can be reduced by 71% (Greenberg et al, 2009)

86% resolution of OSA after gastric bypass (Buchwald et al 2004)

Sleep study / CPAP titration should be repeated after significant weight loss has occurredSlide41

The Obesity hypoventilation syndromeSlide42

Definition of OHS

Awake hypercapnia (PaCO2>45mmHg)

Obese patient (BMI>30)

Exclusion of other causes for hypoventilation (lung disease, neuromuscular disease)

90% of these patients have co-existing OSA

OHS is associated with higher mortality, reduced quality of life, and higher rates of comorbidity (Pulmonary hypertension, heart failure, angina, HTN)Slide43

Which patients have OHS?

0.3-0.4% of the population

10-20% of outpatients presenting to sleep clinics

50% of patients with BMI > 50

OHS patients more likely to have central obesity compared to obese patients without OHSSlide44

Pathogenesis of OHS

Upper airway obstruction during sleep (OSA) leads to increased CO2

Eucapnic

OSA patients are able to normalize their CO2 levels between these events, patients with OHS are not

Rise in bicarbonate levels further blunts

ventilatory

response to rise in CO2

Increased work of breathing due to restrictive effects of obesity

Ventilation / perfusion mismatch

Respiratory muscle impairment

Patients with OHS lack the usual increased

ventilatory

drive seen in patients with obesity

Leptin

resistance (

leptin

normally stimulates ventilation)Slide45

Symptoms of OHS

Many indistinguishable from OSA

Snoring

excessive daytime sleepiness

choking

Pulmonary hypertension / RV dysfunction

JVD

pedal edema

hepatomegalySlide46

Diagnosis of OHS

Awake hypoxemia on pulse

oximetry

High serum bicarbonate can be a clue

Arterial blood gas

PaCO2 > 45

Often hypoxemia with PaO2<70

Normal A-a gradient (widened in lung disease)

Pulmonary function tests and CXR to exclude other diseases

Sleep study to evaluate for OSASlide47

Treatment of OHS

Nocturnal positive airway pressure

BIPAP or CPAP +/- O2 (if necessary)

Goal of eliminating obstructive events at night (if present) and improving alveolar ventilation

Follow up daytime blood gases should be done to see that hypoventilation has improved

Daytime supplemental oxygen

Interventions directed at weight loss

Dietary, pharmacologic, bariatric surgerySlide48

Prognosis of OHS

Patients who are not treated with NIV have a higher mortality

18 months 23%

7 years 46%

Untreated patients have increased levels of daytime sleepiness and reduced quality of lifeSlide49

Obesity and venous thromboembolismSlide50

Obesity and Venous Thromboembolism

Relative risk of DVT in obese: 2.5

Relative risk of Pulmonary embolism in obese: 2.21 (Stein et al 2005)

Association is stronger as BMI increasesSlide51

Potential mechanisms for VTE in obese patients

Increased abdominal fat and intra-abdominal pressure leading to decreased blood velocity in femoral vein

Inactivity/Poor gait

Endothelial dysfunction

Leptin

: leads to higher levels of PAI-1 leading to

prothrombotic

state

Chronic inflammatory state leading to increased thrombosisSlide52

Conclusion

Obesity can have a significant impact on lung function and lead to higher risk of lung diseases

Obesity often leads to chronic dyspnea which can significant impact quality of life

Obstructive sleep apnea and OHS pose a significant health risk; health care providers should try to appropriately screen patients who may benefit from treatment.Slide53

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